Risk of AFib reduced by 6% for each increase in habitual caffeine intake of 300 mg/day
According to the American Heart Association atrial fibrillation (also called AFib or AF) is a quivering or irregular heartbeat (arrhythmia) that can lead to blood clots, stroke, heart failure and other heart-related complications.
The link between habitual caffeine intakes with incident AF was unknown until now. Dr. Dongfeng Gu, MD, PhD, Division of Population Genetics and Prevention, Cardiovascular Institute and Fu Wai Hospital along with colleagues examined the association between chronic exposure of caffeine and the risk of atrial fibrillation (AF). They also investigated the potential dose-response relation.
In this meta-analysis the researchers ha d searched Pubmed, Embase and the Cochrane library up to November 2013 and references of retrieved relevant articles. Prospective cohort studies were included with relative risk or hazard ratio and 95% confidence intervals for AF according to coffee/caffeine intake.
This current analysis includes six prospective cohort studies with a total of 228,465 participants. Three were conducted in the U.S., two in Sweden, and one in Denmark. Caffeine consumption was determined based on daily coffee consumption in three studies and on consumption of coffee, tea, cola, cocoa, or chocolate in the other three.
The amount of caffeine in a cup of coffee varied by geographical location; United Kingdom and Northern Europe 140mg, United States 85mg and Southern Europe 50mg.
Low caffeine intake was considered less than 500mg/day and high intake was over 500mg/day.
During an average follow-up which ranged from 4 to 25.2 years, 1.9% of participants developed AF or had it recorded. (Only four of the studies showed participants free of AF at baseline).
In primary meta-analysis, caffeine exposure was weakly associated with a reduced risk of AF (RR 0.90; 95% CI 0.81 to 1.01, P = 0.07; I2 = 73%).
In the subgroup analysis, pooled results from studies with adjustment of potential confounders showed a 11% reduction for low doses (RR 0.89; 95% CI 0.80 to 0.99, P = 0.032; I2 = 30.9%, P = 0.227) and 16% for high doses (RR 0.84; 95% CI 0.75 to 0.94, P=0.002; I2 = 24.1%, P = 0.267) of caffeine consumption in AF risk.
An inverse relation was found between habitual caffeine intake and AF risk in dose response meta-analysis and the incidence of AF decreased by 6 % for every 300 mg/day increment in habitual caffeine intake.
In their conclusion the researchers write, “In this study, an inverse relation was found between habitual caffeine intake and AF risk by dose-response meta-analysis of prospective cohort studies. It is unlikely that habitual caffeine intake increases AF risk. Potential beneficial effect of habitual caffeine intake on AF needs further research.”
Even though a cause and effect relationship could not be established the researchers hypothesized that caffeine may protect against AF through its anti-fibrotic effect.
The team had written "There were several studies [that] showed that caffeine reduced hepatic fibrosis ... by interfering with transforming growth factor beta signaling.” "Though there are few studies evaluating the anti-fibrosis effect of caffeine on the heart, it is possible that caffeine also prevents cardiac fibrosis."
Protection also "might be related to co-occurring phytochemicals because caffeine is normally consumed in the form of plant-derived products and extracts that invariably contain other potentially bioactive phytochemicals."
This analysis had limitations that included possible underestimation of incident atrial fibrillation, self-reported caffeine intake, the inability to adjust for some potential confounders, such as sleep apnea and the small number of AF events in the studies.
This meta-analysis is published online in the Canadian Journal of Cardiology.